34 articles - From Saturday Mar 26 2022 to Friday Apr 01 2022
Guidelines, position statements, white papers, technical reviews, consensus statements, etc…
meta-analyses and systematic reviews
RCT, clinical trials, retrospective studies, etc…
| Am J Kidney Dis |
Association of Uremic Solutes With Cardiovascular Death in Diabetic Kidney Disease. Higher plasma concentrations and lower U/P ratios of uremic solutes were independently associated with CV and all-cause mortality in DKD. Associations of U/P ratios with mortality suggest a connection between renal uremic solute clearance and CVD pathogenesis. |
| Clin J Am Soc Nephrol |
Acute Kidney Injury in Critically Ill Patients with Cancer. AKI can have major repercussions for patients with cancer, potentially jeopardizing further eligibility for therapy and leading to greater morbidity and mortality. This review highlights the epidemiology of AKI in critically ill patients with cancer, risk factors for AKI, and common pathologies associated with certain cancer therapies, as well as the management of AKI in different clinical scenarios. It highlights gaps in our knowledge of AKI in patients with cancer, including the lack of validated biomarkers, as well as evidence-based therapies to prevent AKI and its deleterious consequences. |
| Clin Kidney J |
Low factor H-related 5 levels contribute to infection-triggered haemolytic uraemic syndrome and membranoproliferative glomerulonephritis. Dysregulation of the alternative complement pathway is a major pathogenic mechanism in two rare renal diseases: atypical haemolytic uraemic syndrome (aHUS) and membranoproliferative glomerulonephritis (MPGN). We report on a 66-year-old male with chronic hepatitis C virus (HCV) infection and a combined liver-kidney transplant that was diagnosed with MPGN at the age of 63 years and a 5-year-old boy who presented with aHUS at the age of 21 |
| J Am Soc Nephrol |
Brief Early Life Angiotensin Converting Enzyme Inhibition Offers Reno-Protection in Sheep with a Solitary Functioning Kidney at 8 Months of Age. Brief and early ACEi in SFK is associated with reduced glomerular hyperfiltration-mediated kidney disease up to 8 months of age in a sheep model. |
Long-term Efficacy and Safety of Repeated Rituximab to Maintain Remission in Idiopathic Childhood Nephrotic Syndrome: An International Study. Children receiving repeated rituximab for FRSDNS experience an improving clinical response. Side effects appear acceptable but significant complications can occur. These findings support repeated rituximab use in FRSDNS. |
| Kidney Int |
Disruption of mitochondrial complex III in cap mesenchyme but not in ureteric progenitors results in defective nephrogenesis associated with amino acid deficiency. In contrast, QPC inactivation in ureteric tree epithelial cells, which give rise to the kidney collecting system, did not inhibit ureteric differentiation, and resulted in the development of functional kidneys that were smaller in size. Thus, our data demonstrate that mitochondrial oxidative metabolism is critical for the formation of cap mesenchyme-derived nephron segments but dispensable for formation of the kidney collecting system. Hence, our studies reveal compartment-specific needs for metabolic reprogramming during kidney development. |
Growth differentiation factor-15 preserves Klotho expression in acute kidney injury and kidney fibrosis. Kidney fibrosis induced by unilateral ureteral obstruction was more severe in Gdf15-deficient mice while GDF15 overexpression decreased kidney injury and preserved Klotho expression. GDF15 increased Klotho expression in vivo in healthy mice, in cultured tubular cells, and prevented Klotho downregulation by inflammatory factors in tubular cells by preventing transcription factor NF- |
Non-canonical Wnt/calcium signaling is protective against podocyte injury and glomerulosclerosis. Mechanistically, specific ablation of Wintless in podocytes caused down-regulation of the nuclear factor of activated T cell 1 (NFAT1) and Nemo-like kinase (NLK), key downstream mediators of non-canonical Wnt/calcium signaling. In vitro, knockdown of either NFAT1 or NLK induced ß-catenin activation while overexpression of NLK significantly repressed ß-catenin induction and largely preserved nephrin in glomerular podocytes. Thus, our results indicate that podocyte-derived Wnts play an important role in protecting podocytes from injury by repressing ß-catenin via activating non-canonical Wnt/calcium signaling. |
The sexual dimorphism of kidney growth in mice and humans. These findings were relevant to humans. Remarkably, by studying living gender-paired kidney donors-recipients, we showed that tubular cell size increased three months after transplantation in men as compared to women, regardless of the donor gender. Thus, our results identify novel signaling pathways that may be involved in androgen-induced kidney growth and homeostasis, and suggest that androgens determine kidney size after transplantation. |
| Nephrol Dial Transplant |
Mechanisms of myostatin and activin A accumulation in chronic kidney disease. During CKD, myostatin and activin A blood concentrations are increased. Myostatin is not overproduced, suggesting only an impaired renal clearance, but activin A is over produced in kidney and heart. We propose to add myostatin and activin A to the list of uremic toxins. |
Plenty of the editorials are available as full text through the publisher website using the provided link
| Am J Kidney Dis |
| Clin J Am Soc Nephrol |
| Kidney Int |
Effects of Acid on Bone. Additionally, there is net proton influx into the mineral with release of bone sodium and potassium. During chronic metabolic acidosis, there is also inhibition of osteoblast activity, resulting in reduced bone formation, and an increase in osteoclast activity, resulting in increased bone resorption and release of calcium and anionic proton buffers. These physicochemical and cell-mediated bone responses to metabolic acidosis, in addition to an acidosis induced increased urine calcium excretion, without a corresponding increase in intestinal calcium absorption, induce a net loss of body calcium which is almost certainly derived from the mineral stores of bone. |
Type I interferon-related kidney disorders. Finally, kidney pathology primarily characterised by vascular lesions (e. g., thrombotic microangiopathy, vasculitis) is a hallmark of the T1I ADA2 deficiency as well as of SLE, viral infections and IFN-therapy. Defining the nosology, pathogenic mechanisms and histopathological patterns of IFN I-related kidney disorders has diagnostic and therapeutic implications, especially considering the likely near-term availability of novel drugs targeting the IFN-I pathway. |
| Nat Rev Nephrol |
Kidney complications of parasitic diseases. The mechanisms that underlie parasitic disease-associated kidney injury include direct parasite damage; immunological phenomena, including immune complex deposition and inflammation; and systemic manifestations such as haemolysis, haemorrhage and rhabdomyolysis. In addition, use of nephrotoxic drugs to treat parasitic infections is associated with acute kidney injury. Early diagnosis of kidney involvement and adequate management is crucial to prevent progression of kidney disease and optimize patient recovery. |
| Nephrol Dial Transplant |
Letters to the editors and authors’ replies
| Am J Kidney Dis |
| J Am Soc Nephrol |
all remaining publications eg case reports, images of the month, etc…
| Am J Kidney Dis |
| Clin J Am Soc Nephrol |
| J Am Soc Nephrol |
| Kidney Int |
| Nat Rev Nephrol |
| Nephrol Dial Transplant |